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Blog / Research Progress / Potential approach to beta cell stress may help lead to type 1 diabetes prevention

Potential approach to beta cell stress may help lead to type 1 diabetes prevention

By Tara Burd

December 6, 2013

Although scientists are still working to determine what causes type 1 diabetes (T1D), research has given us insights into the disease process – knowledge that may eventually lead to potential therapies. One idea that has been explored over the past several years is that of beta cell stress and its connection to T1D, and a recently JDRF-funded study led by the Harvard School of Public Health (HSPH) is giving us new clues into the phenomenon and one possible way to prevent it.

Within a cell, the endoplasmic reticulum (ER) is like a miniature factory where the cell performs some of its specialized functions, like producing proteins. The ER plays a crucial role in the function of pancreatic beta cells, which are responsible for producing, storing, and releasing insulin. However, research has shown that a component of the T1D disease process leads to ER stress, compromising its function and contributing to beta cell death. Could reducing cell stress and improving ER function before disease onset reduce the incidence of T1D? This is what researchers, funded by JDRF and others, set out to explore.

Over the past few years, JDRF has supported research into ER stress, its causes, its implications for T1D, and potential ways to thwart its occurrence. In 2011, a JDRF-funded study was published in Diabetes, showing for the first time evidence of beta cell stress early in the disease process, before a clinical diagnosis of T1D. Building on this information, the latest piece of the puzzle is the HSPH study, published online in the November 13th edition of Science Translational Medicine.

In this study, Dr. Gökhan S. Hotamisligil and his team tested the effects of tauroursodeoxycholic acid (TUDCA) on ER function in mouse models of T1D. TUDCA is a compound that occurs naturally in animal bile, and is similar to a bile acid that occurs naturally in humans. Previous studies by Dr. Hotamisligil’s lab showed that ER stress in other tissues plays a significant role in obesity and type 2 diabetes, and that it can be corrected by compounds such as TUDCA. Those earlier findings propelled the researchers to expand their work into T1D. What they discovered was that the application of TUDCA improved ER function in mice with T1D or pre-diabetes. Beta cells not only functioned better but were more likely to survive, thus preventing the onset of T1D in the animal model tested.

The HSPH study supports one of JDRF’s priority research areas, aimed at beta cell restoration. For a decade, JDRF has funded research to explore ways to maintain and restore the body’s ability to produce insulin and prevent the autoimmune attack that leads to T1D. Piecing together findings from a plethora of studies and human clinical trials will help enrich our understanding of the disease, which will one day lead to a cure.

JDRF is very excited by the outcome of the pre-clinical study and the potential for developing strategies for clinical translation in people with recently diagnosed or early stages of T1D.